This invention relates to the correction of incompetent venous valves or venous valvuloplasty, and more particularly to minimally invasive correction of venous insufficiency using a catheter based system to deploy an appliance or a prosthesis to repair or augment a valve in a vein.
The human venous system of the lower limb consists essentially of the superficial venous system and the deep venous system with perforating veins connecting the two systems. The superficial system includes the great saphenous vein and the small saphenous vein. The deep venous system includes the anterior and posterior tibial veins which unite to form the popliteal vein which in turn becomes the femoral vein when joined by the small saphenous vein. The venous systems contain a plurality of valves for directing blood flow to the heart.
Venous valves are usually bicuspid valves, with each cusp forming a sack or reservoir for blood which, under pressure, forces the free edges of the cusps together to prevent retrograde flow of the blood and allow only antegrade flow to the heart. When an incompetent valve attempts to close in response to a pressure gradient across the valve, the cusps do not seal properly and retrograde flow of blood occurs. There are two chronic venous diseases in which incompetence of venous valves is thought to be an important factor in the pathophysiology. These are varicose veins and chronic venous insufficiency.
Chronic venous insufficiency is a problem caused by hydrodynamic forces acting on the lowest part of the body, the legs, ankles and feet. As the veins dilate due to increased pressure, the valves in the veins become less able to withstand the weight of the blood above them. This causes the veins to dilate further and the valves in the veins to fail. As they fail, the effective height of the column of blood above the feet and ankles grows longer, and the weight increases with an increase in the pressure exerted on the tissues of the ankle and foot. When the weight of that column reaches a critical point because of enough dilation and valve failures, the person begins to have ulcerations of the ankle which start deep and eventually come to the surface. These ulcerations are very difficult to heal because the weight of blood causing them still exists, with the tendency to enlarge the ulcer, and because they are deep, often to the bone.
Chronic venous insufficiency consists of hypertension of the lower limb in the deep, perforating and often superficial veins with associated pigmentation, pain, swelling and ulceration. Existing treatments for chronic venous insufficiency are less than ideal. The only therapies currently available include elevation of the legs for twenty minutes every two hours, elastic support hose to compress the veins externally and surgical repair or replacement of the valves by grafting vein from the person's arm into the leg. These methods are variably effective. Moreover, surgery has its associated complications with risk to life and is usually very expensive. Similarly, the palliative therapies require major lifestyle changes for the patient. Also, without repairing the valves, even if the ulcers are healed, the ulcers always recur unless the patient continues to elevate the legs and to use support hose continuously.
Chronic venous insufficiency is essentially caused by venous hypertension and chronic venous stasis due to valvular incompetence both of a primitive nature (or primary or essential or idiopathic) and of a secondary nature following past illnesses of the venous system (generally speaking, deep venous thrombosis or phlebitis). In the case of venous valvular incompetence, the doctor has no efficacious drugs at his disposal, and the surgeon does not have ready access to artificial venous valves; whereas, valves of various types for heart diseases, etc. have been available for many years. Some methods of valvular reconstructive surgery may allow the recovery of valvular function in certain cases. However, the use of reconstructive surgery is obstructed by the delicate nature and irreversible damage of the valvular structures.
The varicose vein condition consists of dilatation and tortuosity of the superficial veins of the lower limb and resulting cosmetic impairment, pain and ulceration. Primary varicose veins are the result of primary incompetence of the venous valves of the superficial venous system. Secondary varicose veins occur as the result of deep venous hypertension which has damaged the valves of the perforating veins, as well as the deep venous valves.
The initial defect in primary varicose veins often involves localized incompetence of a venous valve thus allowing reflux of blood from the deep venous system to the superficial venous system. This incompetence is traditionally thought to arise at the saphenofemoral junction but may also start at the perforators. Thus, gross saphenofemoral valvular dysfunction may be present in even mild varicose veins with competent distal veins. Even in the presence of incompetent perforators, occlusion of the saphenofemoral junction usually normalizes venous pressure.
The initial defect in secondary varicose veins is often incompetence of a venous valve secondary to hypertension in the deep venous system. Since this increased pressure is manifested in the deep and perforating veins, correction of one site of incompetence could clearly be insufficient as other sites of incompetence will be prone to develop. However, repair of the deep vein valves would correct the deep venous hypertension and could potentially correct the secondary valve failure. Apart from the initial defect, the pathophysiology is similar to that of varicose veins.
Prior art prostheses include artificial venous valves and artificial valves for the heart and other anatomy which are adaptable for use in a vein. One such disclosed venous valve is comprised of an annular support member or ring defining an opening therethrough, including leaflets hingedly attached to the support ring for opening and closing the support ring opening in a manner permitting substantially unidirectional flow therethrough. Such valves are designed to be sutured or sewn into place within a blood vessel during a lengthy open surgery. The support ring of the valve is secured within a flexible fabric tube at a location generally medially of the tube. The blood vessel then is completely severed to provide two free ends; and each end of the fabric tube, within which the valve is secured, is sutured or sewn to a corresponding end of the free blood vessel to effectively splice the blood vessel.
Such prior art valves are likely to result in clotting of blood about the support member of the valve. Such clotting is, of course, undesirable and may be promoted by the fabric tube commonly utilized when suturing the valve into place. In particular, the fabric of the tube normally defines regions or voids within which blood is permitted to accumulate and clot. Furthermore, the fabric of the tube and support ring may provide gaps or spaces between the outer surface of the support ring and the inner wall of the fabric tube. Such gaps may cause the buildup of blood, thereby promoting clotting.